Intensive Lifestyle Changes for Reversal

of Coronary Heart Disease

Dean Ornish, MD; Larry W. Scherwitz, PhD; James H. Billings, PhD, MPH; K. Lance Gould, MD;
Terri A. Merritt, MS; Stephen Sparler, MA; William T. Armstrong, MD; Thomas A. Ports, MD;
Richard L. Kirkeeide, PhD; Charissa Hogeboom, PhD; Richard J. Brand, PhD

Context.—The Lifestyle Heart Trial demonstrated that intensive lifestyle THE LIFESTYLE Heart Trial was the
changes may lead to regression of coronary atherosclerosis after 1 year. first randomized clinical trial to investi-
Objectives.—To determine the feasibility of patients to sustain intensive lifestyle gate whether ambulatory patients could
changes for a total of 5 years and the effects of these lifestyle changes (without be motivated to make and sustain com-
lipid-lowering drugs) on coronary heart disease. prehensive lifestyle changes and, if so,
whether the progression of coronary
Design.—Randomized controlled trial conducted from 1986 to 1992 using a atherosclerosis could be stopped or re-
randomized invitational design. versed without using lipid-lowering
Patients.—Forty-eight patients with moderate to severe coronary heart disease drugs as measured by computer-as-
were randomized to an intensive lifestyle change group or to a usual-care control sisted quantitative coronary arteriogra-
group, and 35 completed the 5-year follow-up quantitative coronary arteriography. phy. This study derived from earlier
Setting.—Two tertiary care university medical centers. studies that used noninvasive mea-
Intervention.—Intensive lifestyle changes (10% fat whole foods vegetarian diet, sures.1,2
aerobic exercise, stress management training, smoking cessation, group psycho- After 1 year, we found that experi-
social support) for 5 years. mental group participants were able to
Main Outcome Measures.—Adherence to intensive lifestyle changes, changes make and maintain intensive lifestyle
changes and had a 37.2% reduction in
in coronary artery percent diameter stenosis, and cardiac events. low-density lipoprotein (LDL) choles-
Results.—Experimental group patients (20 [71%] of 28 patients completed terol levels and a 91% reduction in the
5-year follow-up) made and maintained comprehensive lifestyle changes for 5 frequency of anginal episodes.3 Average
years, whereas control group patients (15 [75%] of 20 patients completed 5-year percent diameter stenosis regressed
follow-up) made more moderate changes. In the experimental group, the average from 40.0% at baseline to 37.8% 1 year
percent diameter stenosis at baseline decreased 1.75 absolute percentage points later, a change that was correlated with
after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points the degree of lifestyle change. In con-
after 5 years (a 7.9% relative improvement). In contrast, the average percent diam- trast, patients in the usual-care control
eter stenosis in the control group increased by 2.3 percentage points after 1 year group made more moderate changes in
(a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% lifestyle, reduced LDL cholesterol lev-
els by 6%, and had a 165% increase in the
relative worsening) (P = .001 between groups. Twenty-five cardiac events occurred frequency of reported anginal episodes.
in 28 experimental group patients vs 45 events in 20 control group patients during Average percent diameter stenosis pro-
the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% con- gressed from 42.7% to 46.1%.
fidence interval, 1.48-4.20]). Given these encouraging findings,
Conclusions.—More regression of coronary atherosclerosis occurred after 5 we extended the study for an additional
years than after 1 year in the experimental group. In contrast, in the control group, 4 years to determine (1) the feasibility
coronary atherosclerosis continued to progress and more than twice as many car- of patients sustaining intensive changes
diac events occurred. in diet and lifestyle for a much longer
JAMA. 1998;280:2001-2007 time, and (2) the effects of these changes
on risk factors, coronary atherosclero-
sis, myocardial perfusion, and cardiac
From the Department of Medicine (Dr Ornish), and Division of Cardiology, University of Texas Medical events after 4 additional years.
the Division of Cardiology (Dr Armstrong), California School, Houston (Drs Gould and Kirkeeide); and the
Pacific Medical Center, San Francisco; the Department Preventive Medicine Research Institue, Sausalito, Calif
of Medicine (Dr Ornish), the Division of Cardiology, (Drs Ornish Scherwitz, and Billings, Mr Sparler, and METHODS
Cardiac Catheterization Laboratory, Cardiovascular Ms Merritt). The design, recruitment, and study
Research Institute (Dr Ports), and the Division of Reprints: Dean Ornish, MD, Preventive Medicine Re-
Biostatistics (Drs Brand and Hogeboom), School of search Institute, 900 Bridgeway, Suite 1, Sausalito, CA population were previously described.3-5
Medicine, University of California, San Francisco; the 94965 (e-mail: DeanOrnish@aol.com). In brief, we recruited men and women

JAMA, December 16, 1998—Vol 280, No. 23 Lifestyle Heart Trial—Ornish et al 2001
©1998 American Medical Association. All rights reserved.
Table 1.—Baseline Characteristics of Experimental and Control Groups*
Experimental
Characteristic
Men, No.
Women, No.
Age, mean (SD), y
Education, mean (SD), y
Employed, No.
Body mass index, mean (SD), kg/m2
No. with history of myocardial infarction
Average No. of lesions studied, mean (SD)
No. with history of percutaneous transluminal
coronary angioplasty
No. with history of coronary artery bypass graft
Reported angina, No. (%)
*Values are statistics unless otherwise indicated. P values are 2-tailed.
with coronary atherosclerosis docu-
mented by quantitative coronary arte-
riography.
We identified 193 patients as poten-
tially eligible for our study who agreed
to undergo quantitative coronary angi-
ography. Following angiography, 93
patients remained eligible and were ran-
domly assigned to experimental or con-
trol groups using a randomized invita-
tional design to minimize crossover,
ethical concerns, nocebo effects, and
dropout. Of these 93 patients who were
eligible, 53 were randomly assigned to
the experimental group and 40 to the
usual-care control group. Patients were
then contacted and invited to participate
in the study; 28 (53%) and 20 (50%)
agreed to participate in the experimen-
tal and control groups, respectively. The
primary reason for refusal in the experi-
mental group was not wanting to un-
dergo intensive lifestyle changes and/or
not wanting a second coronary angio-
gram; control patients refused primarily
because they did not want to undergo a
second angiogram. To detect possible se-
lection biases, we collected data on age,
marital status, reported angina, history
of myocardial infarction, height, weight,
number of diseased lesions, and stenosis
severity for all patients who were ran-
domized into the study but refused to
participate. We did not exclude any ex-
perimental group patients who volun-
teered even if we doubted their ability to
adhere to the lifestyle program. All pa-
tients who volunteered were followed up
using the intention-to-treat principle.
After 1 year, 7 patients did not pro-
vide angiographic data, and the reasons
for loss to follow-up have been reported.3
Of the remaining 41 patients at baseline
most had severe coronary atherosclero-
sis: 28 had 3-vessel disease, 12 had
2-vessel disease, and 1 had 1-vessel
disease. Two of these patients whose
angiographic data were not usable after
1 year agreed to undergo quantitative
coronary arteriography after 5 years;
these results are included in the baseline
2002 JAMA, December 16, 1998—Vol 280, No. 23
©1998 American Medical Association. All rights reserved.
Control P
(n = 20) (n = 15) Value
20 12
.07
0 3
57.4 (6.4) 61.8 (7.5) .08
15.5 (2.7) 14.5 (3.4) .29
14 6 .10
28.4 (4.1) 25.4 (3.5) .03
12 5 .17
5.3 (2.7) 5.3 (3.2) .93
5 4 ..99
1 0 ..99
11 (55) 6 (40) .49
to 5-year comparisons.
Four experimental and 4 control pa-
tients who had an angiogram at 1 year did
not have a third angiogram after 5 years.
Three of these 4 patients in the experi-
mental group refused a third angiogram
(patients only volunteered for a 1-year
study that was subsequently extended),
and 1 died between years 1 and 4; of the 4
control group patients who did not un-
dergo a third angiogram, 1 died, 2 under-
went revascularization of the arterial
lesions under study, and 1 developed
Parkinson disease and became too ill to
be safely tested. Cine arteriograms made
in San Francisco, Calif, were sent to the
University of Texas Medical School,
Houston, for blinded quantitative analy-
ses as previously described in detail.4
All results, except lesion changes at 1
year (18 experimental and 15 control
subjects) and cardiac events after 5
years (all 28 experimental and 20 control
subjects), are based on the total of 35
patients (20 experimental and 15 control
subjects) who had both baseline and 5-
year angiograms. From these 35 pa-
tients, there were 224 lesions studied at
baseline, of which 24 were 100% occluded
and were excluded a priori from the le-
sion-change analyses per the study pro-
tocol. Of the remaining 200 lesions, 14
were lost to the 4-year follow-up, as fol-
lows: in the experimental group, 2 le-
sions were excluded due to technical fail-
ure during the angiogram and 2 had
views that did not match; in the control
group, views did not match for 3 lesions,
3 lesions were excluded due to technical
failure, 1 was excluded due to angio-
plasty, and 3 were excluded due to coro-
nary artery bypass surgery. Of the 186
lesions available for analysis at 4 years,
109 were from the experimental group
and 77 were from the control group.
The 1-year original study and the 4-
year extension were approved by the
committees on human research at Cali-
fornia Pacific Medical Center and Uni-
versity of California, San Francisco, and
each patient signed a written consent
form after being fully informed of the
study requirements.
Patients completed a 3-day diet diary
at baseline and after 1 and 5 years to
assess nutrient intake and dietary ad-
herence.6 Methods of lipid assays were
the same as previously reported.3 These
3-day diet diaries were analyzed with a
software package (CBORD Diet Ana-
lyzer; CBORD Group Inc; Ithaca, NY)
using the US Department of Agricul-
ture database. Also, patients were asked
to complete a questionnaire reporting
the frequency and duration of exercise
and of each stress management tech-
nique. Information from these sources
was quantified into continuous scores us-
ing an a priori determined formula. The
adherence measure was a continuous
score reflecting daily intake of choles-
terol (in milligrams), fat (in grams),
frequency and duration of exercise, fre-
quency and duration of stress manage-
ment techniques, and smoking. A score
of 1.0 equalled 100% adherence but
scores could be greater than 1.0 if par-
ticipants exceeded the recommended in-
tensive lifestyle changes.
The technicians responsible for per-
forming all medical tests were blinded to
patient group assignment. Also, different
personnel implemented the lifestyle in-
tervention, conducted the tests, and com-
putedstatisticalanalyses,althoughthedi-
etitian was made aware of the nutrient
analysis to monitor patients’ safety and
adherence. Quantitative coronary arte-
riograms were blindly analyzed without
knowledge of group assignment.
Program Intervention
Experimental group patients were
prescribed an intensive lifestyle pro-
gram that included a 10%-fat vegetarian
diet, moderate aerobic exercise, stress
management training, smoking cessa-
tion, and group psychosocial support
previously described in detail.3,7-10 Pa-
tients were encouraged to avoid simple
sugars and to emphasize the intake of
complex carbohydrates and other whole
foods. Only 1 patient in the experimental
group was actively smoking at baseline,
and she quit at entry. Control group pa-
tients were asked to follow the advice of
their personal physicians regarding life-
style changes.
Statistical Methods
We decided a priori to use percent di-
ameter stenosis as the primary depen-
dent variable. Statistical methods to
compare the 2 groups were previously
described.3 Analysis of adherence vari-
ables and risk factor levels used time-
structured repeated measures in which
levels from all 3 measurement times
(baseline, 1 year, and 5 years) were in-
Lifestyle Heart Trial—Ornish et al
Table 2.—Adherence to Exercise, Stress Management, and Dietary Guidelines

Mean (SEM) at Baseline Mean (SEM) at 1 Year Mean (SEM) at 5 Years

Experimental Control Experimental Control P Value* Experimental Control P Value*

(n = 20) (n = 15) (n = 20) (n = 15) Baseline-1 Year (n = 20) (n = 15) Baseline-5 Years
Exercise
Times per week 2.66 (0.84) 2.38 (0.77) 4.97 (0.35) 2.87 (0.70) .06 4.34 (0.49) 3.57 (0.56) .64
Hours per week 2.26 (0.85) 2.42 (0.99) 5.02 (0.61) 2.52 (0.70) .12 3.56 (0.56) 2.90 (0.65) .50
Stress management
Times per week 0.70 (0.41) 0.15 (0.10) 8.22 (0.73) 0.49 (0.25) ,.001 4.93 (1.02) 0.74 (0.39) ,.001
Minutes per day 6.01 (3.56) 1.71 (1.19) 87.25 (7.85) 4.47 (2.79) ,.001 48.53 (10.36) 8.44 (6.11) .001
Fat intake
Grams per day 63.67 (4.35) 57.42 (5.94) 12.71 (1.06) 52.38 (5.31) ,.001 17.34 (2.30) 44.09 (6.66) ,.001
% of Energy intake 29.71 (1.8) 30.52 (2.9) 6.22 (0.3) 28.76 (2.3) ,.001 8.51 (1.0) 25.03 (2.7) ,.001
Dietary cholesterol, mmol/L [mg/dL] 5.47 (0.672) 5.49 (0.908) 0.08 (0.002) 4.69 (0.636) ,.001 0.48 (0.140) 3.59 (0.641) .002
[211.4 (26.0)] [212.5 (35.1)] [3.3 (0.8)] [181.3 (24.6)] [18.6 (5.4)] [138.7 (24.8)]
Energy intake, J/d 8159 (473) 7159 (489) 7623 (473) 7004 (489) .64 7724 (485) 6581 (489) .86
Total adherence score† 0.62 (0.08) 0.60 (0.07) 1.29 (0.08) 0.64 (0.07) ,.001 1.06 (0.08) 0.72 (0.07) ,.001

*All P levels are 2-tailed and each is a result of a test of the null hypothesis that the change between 2 particular visits (eg, baseline and 1 year) does not differ between
the experimental and control groups.
†Percentage of minimum recommended level of combined lifestyle change; includes all the above plus smoking cessation.

Table 3.—Baseline Levels, 1-Year, and 5-Year Change Scores in Coronary Artery Lesions*

Mean at Baseline (95% CI) Change Scores at 1 Year (95% CI) Change Scores at 5 Years (95% CI)

Experimental Control Experimental Control P Value† Experimental Control P Value†

(n = 20) (n = 15) (n = 18) (n = 15) Baseline-1 Year (n = 20) (n = 15) Baseline-5 Years
Diameter stenosis, % 38.92 42.50 −1.75 2.28 .02 −3.07 11.77 .001
(35.29 to 42.54) (38.18 to 46.81) (−4.08 to 0.58) (−3.0 to 4.86) (−5.91 to −0.24) (3.40 to 20.14)
Minimum diameter, mm 1.64 1.74 0.01 −0.12 .11 0.001 −0.34 .05
(1.44 to 1.84) (1.50 to 1.97) (−0.10 to 0.12) (−0.25 to −0.001) (−0.11 to 0.11) (−0.66 to −0.02)
Normal diameter, mm 2.65 2.96 −0.06 −0.10 .68 −0.13 0.045 .01
(2.39 to 2.92) (2.64 to 3.27) (−0.16 to 0.03) (−0.27 to 0.06) (−0.26 to 0.01) (0.017 to 0.072)

*CI indicates confidence interval.

†All P levels are 2-tailed and each is a result of a test of the null hypothesis that the change between 2 particular visits (eg, baseline and 1 year) does not differ between
the experimental and control groups.

cluded in a single regression model. Sta-
tistical significances of group differences
were obtained for baseline levels, 1-year
changes, and 5-year changes using F
tests. All repeated measures analyses
were implemented using PROC MIXED
under SAS version 6.08.11 Analysis of le-
sion data used a repeated measures
model in which the repeated measures
were baseline or change values for mul-
tiple lesions within each subject. Change
scores were used for the baseline to 1-
year and baseline to 5-year follow-up pe-
riods, and analysis of baseline levels, 1-
year changes, and 5-year changes were
done separately. Again, F tests provided
by SAS PROC MIXED were used to test
significance of differences between
groups with respect to baseline levels,
1-year changes, and 5-year changes. The
SAS PROC MIXED linear regression,
which allowed for dependence in data,
was used to determine the relationship
between adherence and percent diam-
eter stenosis changes. Relative rates for
cardiac events were analyzed and tested
by Poisson regression using exact tests
(Stata 5.0, College Station, Tex).
RESULTS
Baseline Comparisons
of Volunteers With Refusals
Those who declined the invitation to
be in the study were similar to those who
volunteered in all available data except
those who volunteered were more likely
to have a history of angina (87% vs 65%;
P = .02), a greater number of lesions (4.5
vs 3.5; P = .04), and slightly more se-
verely stenosed lesions (2.3 vs 2.0 on a
3-point scale; P = .05).
Baseline Comparisons
of Experimental Group
With Control Group
Analyses across the 35 volunteers at
baseline for whom 4-year lesion data
were available showed no significant dif-
ferences between the experimental
group and the control group in demo-
graphic characteristics, history of myo-
cardial infarction, angioplasty, bypass
surgery, lesion number, lesion stenosis,
dietary fat or cholesterol intake, exer-
cise and stress management practice,
blood pressure, exercise capacity, and
psychosocial measures (Tables 1-3).
Among the many comparisons, only a
few differed significantly (P,.05). More
women were randomly assigned to the
control group (4) than to the experimen-
tal group (1); this fact accounted for half
the weight difference (10 kg) between
the 2 groups and most of the height dif-
ference (6 cm).
Experimental group patients had a
slightly larger body mass index (mea-
sured as the weight in kilograms divided
by the square of the height in meters)
(28.4 vs 25.4 kg/m2; P = .03) and had lower
high-density lipoprotein (HDL) choles-
terol levels (1.04 mmol/L [40.1 mg/dL] vs
1.36 mmol/L [52.4 mg/dL]; P = .04),
which was also reflected in lower apoli-
poprotein A-I levels (3.45 mmol/L [133.1
mg/dL] vs 4.08 mmol/L [157.5 mg/dL];
P = .03). The lower body mass index in
the control group may be due to the
larger number of women in the control
group. Other lipid values, including ra-
tios of total cholesterol to HDL and LDL
to HDL, did not differ significantly at
baseline (Table 4).
Program Adherence
In the experimental group, adherence
to all aspects of the program was excel-
lent during the first year and good after 5
years, whereas control group patients
maintained more moderate changes dur-
ing the 5 years consistent with conven-
tional guidelines (Table 2). The percent-
age of daily energy (calories) provided by
fruits, vegetables, whole grains, soy,
other legumes, nonfat dairy, and alcohol
was comparable at 1 year and at 5 years.
In the experimental group, fat intake
decreased from approximately 30% to
8.5%, cholesterol from 211 to 18.6 mg/d,
energy from 8159 to 7724 J (1950-1846
cal), protein from 17% to 15%, and carbo-
hydrates increased from 53% to 76.5%. In

JAMA, December 16, 1998—Vol 280, No. 23 Lifestyle Heart Trial—Ornish et al 2003
©1998 American Medical Association. All rights reserved.
Table 4.—Changes in Risk Factors

Mean (SEM) at Baseline Mean (SEM) at 1 Year

Experimental Control Experimental Control

Risk Factor (n = 20) (n = 15) (n = 20) (n = 15)
Serum lipids, mmol/L [mg/dL]
Total cholesterol 5.83 (0.31) [225.1 (11.9)] 6.42 (0.24) [247.9 (9.4)] 4.22 (0.22) [162.9 (8.4)] 6.33 (0.38) [244.3 (14.7)]
Low-density lipoprotein 3.72 (0.29) [143.80 (11.21)] 4.30 (0.19) [166.40 (7.46)] 2.24 (0.24) [86.56 (9.41)] 4.25 (0.38) [164.13 (14.85)]
High-density lipoprotein 1.04 (0.07) [40.05 (2.78)] 1.36 (0.14) [52.36 (5.54)] 0.94 (0.10) [36.28 (3.81)] 1.34 (0.10) [51.87 (3.81)]
Triglyceride 5.90 (0.69) [227.8 (26.5)] 5.78 (1.63) [223.3 (63.0)] 6.69 (0.75) [258.2 (29.1)] 4.30 (0.40) [166.1 (15.5)]
Apolipoproteins, g/L
A-I 1.331 (0.046) 1.575 (0.092) 1.308 (0.057) 1.761 (0.121)
B 1.000 (0.054) 1.024 (0.062) 0.7685 (0.046) 1.085 (0.053)
Blood pressure, mm Hg
Systolic 135.3 (4.0) 137.2 (4.5) 126.4 (3.9) 128.8 (4.5)
Diastolic 81.70 (2.05) 80.27 (3.15) 77.03 (2.01) 75.07 (8.15)
Weight, kg 91.40 (3.42) 75.74 (4.37) 80.64 (2.48) 77.18 (4.73)

*All P levels are 2-tailed and each is a result of a test of the null hypothesis that the change between 2 particular visits (eg, baseline and 1 year) does not differ between
the experimental and control groups.

Table 5.—Reported Angina Symptoms

Mean (SD) at Baseline Mean (SD) at 1 Year Mean (SD) at 5 Years

Experimental Control Experimental Control P Value* Experimental Control P Value*

(n = 18) (n = 14) (n = 18) (n = 14) Baseline-1 Year (n = 18) (n = 14) Baseline-5 Years
Chest pain frequency, times per week 5.8 (14.7) 1.4 (1.8) 0.5 (0.8) 4.0 (9.3) .08 1.6 (2.7) 0.9 (1.9) .32
Chest pain duration, min 3.1 (4.8) 3.2 (8.4) 1.8 (4.7) 7.6 (15.9) .11 0.9 (1.3) 1.0 (2.7) .93
Chest pain severity (1-7 scale) 1.5 (1.5) 0.6 (0.8) 0.7 (1.2) 1.4 (1.2) ,.001 0.9 (1.4) 0.6 (1.1) .29

*All P levels are 2-tailed and each is a result of a test of the null hypothesis that the change between 2 particular visits (eg, baseline and 1 year) does not differ between
the experimental and control groups.

the control group, fat intake decreased
from 30% to 25%, cholesterol from 212.5
to 138.7 mg/d, energy from 5.49 to 3.59 J
(1711-1573 cal), protein from 19% to 18%,
and carbohydrates increased from 51% to
52%. Since patients volunteered origi-
nally only for a 1-year study, there was a
significant decrease in meeting atten-
dance after 1 year for 4 of the patients.
Walking was the recommended form of
exercise, but some patients jogged or did
more strenuous exercise.
Risk Factor Changes
Patients in the experimental group
lost 10.9 kg (23.9 lbs) at 1 year and sus-
tained a weight loss of 5.8 kg (12.8 lbs) at
5 years, whereas weight in the control
group changed little from baseline. In
the experimental group, LDL choles-
terol levels decreased by 40% at 1 year
and remained 20% below baseline at 5
years. In the control group, LDL choles-
terol levels decreased by 1.2% at 1 year
and by 19.3% at 5 years. There were no
statistically significant differences in
LDL levels between the 2 groups at 5
years, primarily because 9 (60%) of
15 control patients took lipid-lowering
drugs between year 1 and year 5 of the
study. None of the experimental group
patients took lipid-lowering drugs dur-
ing the 5 years of the study. Fourteen
patients in the experimental group and
11 patients in the control group took as-
pirin during the study.
Triglycerides did not change signifi-
cantly in either group. Apolipoprotein
A-I did not change in the experimental
group, but it increased in the control
group (P = .04). High-density lipoprotein
levels and blood pressure did not differ
between the 2 groups.
Angina Pectoris
Experimental group patients had a
91% reduction in reported frequency of
angina after 1 year and a 72% reduction
after 5 years (Table 5). In contrast, con-
trol group patients had a 186% increase
in reported frequency of angina after 1
year and a 36% decrease in frequency
after 5 years. The decrease in angina in
the control group after 5 years was in
large part because 3 of the 5 patients
who reported an increase in anginal epi-
sodes from baseline to 1 year underwent
coronary angioplasty between years 1
and 5. Because of this reduction in angina
in control group patients who under-
went revascularization, the between-
group differences were no longer signifi-
cant after 5 years (Table 5).
Angiographic Changes
All detectable lesions that matched at
baseline and 5-year follow-up and were
not 100% occluded at baseline were in-
cluded in the analyses (n = 186). At base-
line, there were no significant differ-
ences between the experimental and
control groups in any measure of lesion
severity (Table 3). In the experimental
group, the average percent diameter
stenosis at baseline decreased 1.75 ab-
solute percentage points after 1 year (a
4.5% relative improvement) and by 3.1
absolute percentage points after 5 years
(a 7.9% relative improvement). In con-
trast, the average percent diameter ste-
nosis in the control group increased by
2.3 percentage points after 1 year (a 5.4%
relative worsening) and by 11.8 percent-
age points after 5 years (a 27.7% relative
worsening). These between-group dif-
ferences were statistically significant af-
ter both 1 year and 5 years (P = .02 and
P = .001, respectively, Figure 1).
Figure 2 shows the experimental
group changes in percent diameter ste-
nosis from baseline to 5 years according
to tertiles of adherence to the lifestyle
intervention. As seen at 1 year,3 there
was also a strong correlation between
adherence and percent diameter steno-
sis after 5 years in a dose-response rela-
tionship; the tertile of patients that was
most adherent to the program had the
most regression, the tertile with inter-
mediate adherence had less regression,
and the tertile with the least adherence
halted the progression of disease with-
out regression (P = .04). Of interest is
that this relationship was not related to
age or disease severity. There was no
significant relationship between adher-
ence and lesion changes in the control
group, perhaps because many of these
patients began taking lipid-lowering
drugs, which may have confounded the
ability to detect a possible relationship.
Indeed, we found significant correla-
tions between changes in lipid levels
(LDL and total cholesterol) and changes

2004 JAMA, December 16, 1998—Vol 280, No. 23 Lifestyle Heart Trial—Ornish et al

©1998 American Medical Association. All rights reserved.

 Mean (SEM) at 5 Years 60

P Value* Experimental Control P Value* †

Baseline-1 Year (n = 20) (n = 15) Baseline-5 Years
55
.004 4.87 (0.20) [188.0 (7.8)] 5.62 (0.20) [217.0 (7.9)] .60
51.9
.003 2.99 (0.20) [115.35 (7.59)] 3.47 (0.21) [133.80 (8.25)] .76

Diameter Stenosis, %
50
.35 0.90 (0.05) [34.75 (2.03)] 1.28 (0.12) [49.27 (4.47)] .54 Control
.17 6.11 (0.59) [236.1 (22.9)] 5.48 (0.78) [211.5 (30.2)] .78

45 ∗
.11 1.302 (0.092) 1.839 (0.139) .04
.004 1.014 (0.072) 0.991 (0.083) .63 42.3
41.3

.96 130.0 (3.9) 123.3 (4.7) .19 40 40.7

.91 76.63 (2.01) 73.61 (3.25) .74

38.5 37.3
.001 85.64 (2.88) 77.09 (4.5) .001
35
Treatment

in lesions in both groups. These correla- duction (continued improvement) after 30

tions remained significant when exam-
ining either the lipid values at 5 years or
the change in lipid values from baseline
to 5 years.
As a secondary analysis, we examined
the results in control group patients who
began taking lipid-lowering drugs during
the study. Percent diameter stenosis pro-
gressed from 45.7% to 51.7%, a change of
Baseline 1y 5y
5 years than after 1 year in experimental
group patients who were asked to make
Figure 1.—Mean percentage diameter stenosis in
intensive lifestyle changes. In contrast, treatment and control groups at baseline, 1 year,
control group patients showed much and 5 years. Error bars represent SEM; asterisk,
more progression (continued worsening) P = .02 by between-group 2-tailed test; dagger,
in average percent diameter stenosis af- P = .001 by between-group 2-tailed test.
ter 5 years than after 1 year, even though
more than half of the control group pa-
tients were prescribed lipid-lowering
–8

Changes in Diameter Stenosis (Baseline to 5 y), %

6.0 absolute percentage points. In the con-
trol patients who did not take lipid-low-
ering drugs the disease progressed from
40.7% to 59.7%, a much greater change of
19.0 absolute percentage points. (No ex-
perimental group patients took lipid-low-
ering drugs during the study.)
The change in body mass index from
baseline to 1 year (r = −0.85; P,.001)
and from baseline to 5 years (r = −0.72;
P = .001) was significantly correlated with
the change in percent diameter stenosis
in the control group only. In other words,
those who gained weight were more likely
to show progression of atherosclerosis.
Cardiac Events
Data on cardiac events were obtained
from all 48 patients. Cardiac events in-
cluded myocardial infarction, coronary
angioplasty, coronary artery bypass sur-
gery, cardiac-related hospitalizations,
and cardiac-related deaths. At 5 years,
there were more cardiac events in the
control group (45 events for 20 patients,
or 2.25 events per patient) than the ex-
perimental group (25 events for 28 pa-
tients, or 0.89 events per patient) (Table
6). Control group patients were more
likely to have undergone coronary angi-
oplasty and bypass surgery and/or to
have been hospitalized for cardiac-re-
lated problems than were experimental
group patients.
COMMENT
The primary end point of this study,
chosen a priori, was percent diameter
stenosis. On average, there was more re-
medications during the course of the
study. Although the sample size was –7 – 6.81
relative small,12 these differences were
statistically significant at both 1 year –6
and 5 years. These findings support the
–5
feasibility of intensive lifestyle changes
in delaying, stopping, or reversing the –4
progression of coronary artery disease
– 3.02
in ambulatory patients over prolonged –3
periods.
We found more than twice as many –2
cardiac events per patient in the control –1
group than in the experimental group. – 0.37
These findings are consistent with other 0
clinical trials showing that even small
changes in percent diameter stenosis are 1
Most Medium Least
often accompanied by marked reduc- Adherence Adherence Adherence
tions in cardiac events.13-16 Other studies (1.60-1.20) (1.18-0.83) (0.73-0.47)
have demonstrated how quickly the [n = 6] [n = 7] [n = 6]
coronary artery endothelium stabilizes
in response to lipid-lowering drugs.17,18 Figure 2.—Changes in percentage diameter steno-
Although there was some reduction in sis by 5-year adherence tertiles for the experimen-
adherence to the intensive lifestyle in- tal group.
tervention between years 1 and 5 in the
experimental group, long-term adher- population.19 In contrast, the Step II diet
ence remained remarkably high in this reduces LDL cholesterol by only 5% or
sample of self-selected patients. The less.20,21
level of lifestyle change, even at 5 years, High-density lipoprotein levels de-
is greater than in any other published creased and triglycerides increased in
study of ambulatory populations. These experimental group patients overall, al-
results are especially encouraging be- though the ratio of LDL to HDL was
cause these patients initially volun- improved. Recent reports assert that
teered to participate for only 1 year this phenomenon, which is often seen in
when they entered the study. very low-fat diets, may be harmful.22,23
The experimental group reduced LDL However, patients in the Lifestyle
cholesterol levels by 40% at 1 year and by Heart Trial showed even more regres-
20% after 5 years; these reductions are sion of coronary atherosclerosis after 5
comparable with those achieved with years than after 1 year as well as signifi-
lipid-lowering drugs in an ambulatory cantly decreased cardiac events. Low

JAMA, December 16, 1998—Vol 280, No. 23 Lifestyle Heart Trial—Ornish et al 2005
©1998 American Medical Association. All rights reserved.
Table 6.—Cardiac Events During 5-Year Follow-up
No. of Events
Experimental* Control† Risk 95% Confidence
(n = 28) (n = 20) Ratio Interval
Myocardial infarction 2 4 2.74 0.393-30.3
Percutaneous transluminal 8 14 2.40 0.939-6.60
coronary angioplasty
Coronary artery bypass graft 2 5 3.43 0.561-36.0
Cardiac hospitalizations‡ 23 44 2.62 1.55-4.55
Deaths 2 1 0.685 0.012-13.2
Any event 25 45 2.47 1.48-4.20
*Person-years of observation was 108.04.
†Person-years of observation was 78.81.
‡Includes myocardial infarction, percutaneous transluminal coronary angioplasty, and coronary artery bypass
graft.
HDL cholesterol levels due to reduced eter remained stable in the experimental
fat intake are the result of a decreased group but markedly narrowed in the con-
transport rate rather than the increased trol group during the 5 years of the study.
catabolism that is responsible for most At 5 years, the differences between the
cases of low HDL cholesterol levels in experimental and control groups were
persons consuming a typical Western statistically significant for both percent
diet.24 Populations consuming low-fat, diameter stenosis and minimum diam-
plant-based diets have low HDL choles- eter, even though control group pa-
terol levels and low rates of coronary tients reported risk reduction behavior
heart disease. Our data provide evidence consistent with a Step II diet of the Na-
using quantitative coronary arteriogra- tional Cholesterol Education Program
phy in this population that diet-induced and the American Heart Association:
lowering of HDL cholesterol does not they consumed an average of 25% of en-
confer the same risk of atherosclerosis ergy (calories) from fat and exercised an
as do low HDL cholesterol levels in average of 3.5 times per week. These data
Americans consuming a high-fat diet.25 are consistent with other studies indi-
Experimental group patients whose tri- cating that moderate changes in diet and
glycerides increased during the first lifestyle may not be sufficient to stop the
year were asked to minimize their in- progression of coronary atherosclerosis
take of simple carbohydrates, and tri- unless combined with lipid-lowering
glyceride levels decreased between year drugs.27
1 and year 5. After 5 years, the normal diameter
The experimental group’s marked re- (the segment of least narrowing proxi-
duction in frequency, severity, and du- mal to the minimum diameter) de-
ration of angina after 1 year was sus- creased slightly in the experimental
tained at similar levels after 5 years. This group but widened slightly in the control
long-term reduction in angina is compa- group. A slight decrease in normal diam-
rable with that achieved following coro- eter, at least up to a point, may improve
nary artery bypass surgery or angio- myocardial perfusion by streamlining
plasty and helps to maintain long-term flow—decreasing the forward flow
adherence.26 Between-group differences losses that occur when going from a
in most measures of chest pain were not larger to a sharply reduced lumen diam-
statistically significant after 5 years be- eter.4 Conversely, the slight increase in
cause there was a large variability in an- the normal diameter and reduction in the
gina and control group patients who minimum diameter seen in control group
were the most symptomatic underwent patients increased the entry angle, fur-
revascularization. ther reducing blood flow. These theoreti-
When we began this study, we be- cal considerations are consistent with
lieved that the younger patients with the substantially increased myocardial
milder disease would be more likely to perfusion in the experimental group and
show regression, but we did not find this decreased myocardial perfusion in the
to be true. Instead, we found that the pri- control group that we measured using
mary determinant of change in percent cardiac positron emission tomography
diameter stenosis in the experimental scans.5
group was neither age nor disease se- A much earlier study by Morrison28
verity but adherence to the recom- found that moderate reductions in fat and
mended changes in diet and lifestyle. This cholesterol intake improved cardiac sur-
relationship of adherence to percent di- vival: after 12 years, all of the control
ameter stenosis in the experimental group patients had died compared with
group was found after 1 year3 and also af- only 62% of experimental group pa-
ter 5 years in a dose-response relation- tients in a nonrandomized trial. More re-
ship. Coronary artery minimum diam- cently, an important study by Esselstyn
2006 JAMA, December 16, 1998—Vol 280, No. 23
©1998 American Medical Association. All rights reserved.
et al29 reported that a similar diet plus
lipid-lowering drugs in 11 patients caused
regression of 11 lesions and stabilization
P in the remaining 14 lesions after 5.5 years.
Value
Although there was no control group,
.26
those who were adherent to the diet re-
,.05
ported substantially fewer cardiac events
.14 than those who were not adherent.29
,.001 Like all clinical trials, our study has
.81 limitations. Although the study partici-
,.001 pants were a diverse group, they may
not be representative of the general
population of patients with coronary
heart disease. Half of the patients who
underwent quantitative coronary arte-
riography in the participatory hospitals
did not meet all of the inclusion and ex-
clusion criteria and were not invited to
participate in the study. Also, half of the
patients who were invited declined to
enroll in the study. Nevertheless, it is
encouraging that 50% of the patients who
were contacted agreed to volunteer de-
spite the requirement for repeated arte-
riography and that experimental group
patients were able to make and maintain
comprehensive lifestyle changes. The
angiographic measures lost to follow-up
may have affected the treatment and con-
trol groups differently, although there
are no data to suggest that this occurred.
In addition, there is a possibility of dif-
ferential loss of lesions in patients, al-
though no evidence indicates that this oc-
curred; in both groups, there were 14 le-
sions that were lost to follow-up. Also, 4
lesions were lost in the control group to
bypass surgery or angioplasty; since
these lesions were worsening sufficiently
to require revascularization, the exclu-
sion of these lesions from analysis would
make between-group differences more
difficult to detect. We recently completed
a multicenter demonstration project to
assess the practicality and cost-effective-
ness of this intervention in a larger
sample of economically and geographi-
cally diverse patients with coronary
heart disease.30
Although we did not use lipid-
lowering drugs in the experimental
group, their value has been demon-
strated in studies that have been pub-
lished since the Lifestyle Heart Trial be-
gan. We do not know if experimental
group patients may have demonstrated
even more improvement by including
lipid-lowering drugs.14-16 Patients in the
control group who were not prescribed
lipid-lowering drugs during the study
showed more than 3 times as much pro-
gression in percent diameter stenosis as
those who were. No experimental group
patients took lipid-lowering drugs dur-
ing the study, yet they showed better re-
sults than control group patients who
were taking these drugs. Lipid-
lowering drugs are expensive, compli-
Lifestyle Heart Trial—Ornish et al
ance is difficult to achieve,31 and long-
term safety is unknown.32 In practice,
patients may be offered a range of thera-
peutic options, including comprehen-
sive lifestyle changes, lipid-lowering drug
therapy, and revascularization, either
separately or in combination.
In summary, these ambulatory pa-
tients were able to make and maintain
comprehensive changes in diet and life-
style for 5 years and showed even more
regression of coronary atherosclerosis af-
ter 5 years than after 1 year as mea-
sured by percent diameter stenosis. In
contrast, patients following more con-
ventional lifestyle recommendations
showed even more progression of coro-
nary atherosclerosis after 5 years than
after 1 year, and had more than twice as
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many cardiac events as patients making
comprehensive lifestyle changes.
Major support for this study was provided by
grants from the National Heart, Lung, and Blood
Institute of the National Institutes of Health,
Bethesda, Md (RO1HL42554), the Department of
Health Services of the State of California, Sacra-
mento (1256SC-01), The Henry J. Kaiser Family
Foundation, Menlo Park, Calif, Gerald D. Hines In-
terests, Houston, Tex, Houston Endowment Inc,
Houston, The John E. Fetzer Institute, Kalamazoo,
Mich, The Nathan Cummings Foundation, New
York, NY, The Bucksbaum Foundation, Des
Moines, Iowa, Gross Foundation, Houston, Pritzker
Foundation, Chicago, Ill, The Enron Foundation,
Houston, the Milken Family Foundation, Los An-
geles, Calif, The Bomer Foundation, Houston, Con-
tinental Airlines, Houston, the Credit Suisse First
Boston Foundation, New York, the Groppe Foun-
dation, Houston, the Ray C. Fish Foundation, Hous-
ton, the Moldaw Philanthropic Fund, Atherton,
Calif, the Dawson Foundation, Cleveland, Ohio, the
12. Ornish D. More on low-fat diets. N Engl J Med.
1998;338:1623-1624.
13. Brown BG, Alberts JJ, Fisher LD, et al. Regres-
sion of coronary artery disease as a result of intensive
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lipoprotein B. N Engl J Med. 1990;323:1289-1298.
14. Jukema JW, Bruschke AVG, Van Boven AJ, et
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gression and regression of coronary artery disease
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4444 patients with coronary heart disease. Lancet.
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Glenn Foundation, Santa Barbara, Calif, Corporate
Property Investors, New York, NY, the Seretean
Foundation, Boca Raton, Fla, the Weatherhead
Foundation, Cleveland, the Texas Commerce Bank
Foundation, Houston, and Arthur Andersen & Co,
Houston.
We are indebted to the following who performed
quanitative coronary arteriography for this study:
Robert Bernstein, MD, Craig Brandman, MD,
Bruce Brent, MD, Ralph Clark, MD, Keith Cohn,
MD, James Cullen, MD, Richard Francoz, MD, Kent
Gershengorn, MD, Gabriel Gregoatos, MD, Lester
Jacobsen, MD, Myron Marx, MD, Patricia McK-
enna, MD, Roy Meyer, MD, Gerald Needleman, MD,
Gene Shafton, MD, Brian Strunk, MD, Anne
Thorson, MD, and John Wack, MD, as well as the
head angiography nurses Georgie Hesse, RN, and
LaVeta Luce, RN. Dale Jones, RT, and Yvonne
Stuart, RT, provided technical support for the arte-
riographic analyses. Special appreciation to Jean-
Marc Fullsack for food services and to Marjorie
McClain and Myrna Melling for administrative
support.
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LDL cholesterol. N Engl J Med. 1998;339:12-20.
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Lifestyle Heart Trial—Ornish et al 2007
LETTERS
counseling and testing data system was begun, and 1 (Florida)
began HIV reporting very recently and not enough time has
elapsed to have adequate data for analysis. The year-to-year me-
dian percentage changes in total number of HIV tests during
1992 through 1996 for areas with and without HIV reporting
were similar in magnitude and trend.2
Although we showed no large declines in testing among MSM
and other risk groups after HIV reporting, we agree with Aragón
and Myers and Dr Woods and colleagues that trends in some sub-
groups—for example, in a small number of MSM concerned with
reporting issues—could be hidden within the larger community
of MSM. Because there will always be individuals concerned about
these issues, we emphasized the importance of making anony-
mous testing available to promote knowledge of HIV status among
at-risk people. The approval by the US Food and Drug Admin-
istration of home sample collection tests for HIV expands the avail-
ability of anonymous testing in all areas.3
Woods et al also state that, except for New Jersey, we in-
cluded only low-prevalence states. This is incorrect. Louisi-
ana (acquired immunodeficiency syndrome [AIDS] rate of 33.7
per 100 000 in 1997) and Tennessee (25.1 per 100 000) have
high AIDS incidence, comparable with their own state of Cali-
fornia (29.8 per 100 000)1 and are considered moderate-
prevalence states.
Dr Solomon and colleagues are concerned that the study de-
sign was ecological and subject to the fallacy inherent in such
studies, ie, that ecological correlations cannot be validly substi-
tuted for individual correlations. However, to demonstrate the
impact of a policy change on a large population, ecological meth-
ods may be the most practical design. In an individual-level study,
each individual’s awareness of the change in policy would be de-
termined. On a population basis, this would be a difficult study
to conduct, especially if attitudes of high-risk persons were to
be assessed. Although our study cannot distinguish between
people who were aware (“exposed”) and unaware (“not ex-
posed”) of the change in reporting policy, the important fact re-
mains that no large changes in testing behavior were observed
1380 JAMA, April 21, 1999—Vol 281, No. 15
in the population. Our results are supported by a recent study
of more than 2500 people in high-risk groups (MSM, IDUs, and
attendees of sexually transmitted disease clinics) in 9 states.4 In
this study, more than 60% of participants were unaware of their
state’s HIV reporting policy and, of those avoiding testing, only
2% stated that reporting was a main factor for not being tested.4
Furthermore, as Dr Paul and colleagues demonstrated in New
Jersey, large numbers of people did not go to nearby states to be
tested after HIV reporting was implemented.
Allyn K. Nakashima, MD
Rosemarie Horsley
Robert L. Frey, PhD
Patricia A. Sweeney, MPH
J. Todd Weber, MD
Patricia L. Fleming, PhD
Centers for Disease Control and Prevention
Atlanta, Ga
1. Centers for Disease Control and Prevention. HIV/AIDS Surveillance Report. At-
lanta, Ga: Centers for Disease Control and Prevention; 1997;9(No.2):32.
2. Centers for Disease Control and Prevention. HIV Counseling and Testing in
Publicly Funded Sites: 1996 Annual Report. Atlanta, Ga: Centers for Disease Con-
trol and Prevention; 1998:17.
3. Branson B. Home sample collection tests for HIV infection. JAMA. 1998;280:
1699-1701.
4. Centers for Disease Control and Prevention. HIV testing among populations at
risk for HIV in nine states: results from the HIV testing survey (HITS), November
1995-December 1996. MMWR Morb Mortal Wkly Rep. 1998;47:1086-1091.
CORRECTIONS
Author Omitted: In the Original Contribution entitled “Intensive Lifestyle Changes
for Reversal of Coronary Heart Disease” published in the December 16, 1998, is-
sue of THE JOURNAL (1998;280:2001-2007), the name of Shirley E. Brown, MD,
was omitted from the list of authors. The full list of authors should read “Dean
Ornish, MD; Larry W. Scherwitz, PhD; James H. Billings, PhD, MPH; Shirley E. Brown,
MD; K. Lance Gould, MD; Terri A. Merritt, MS; Stephen Sparler, MA; William T.
Armstrong, MD; Thomas A. Ports, MD; Richard L. Kirkeeide, PhD; Charissa Ho-
geboom, PhD; Richard J. Brand, PhD.”
Incorrect Location: In the MSJAMA Essay entitled “Physician-Legislators: Physi-
cians Practicing Public Service” published in the March 3, 1999, issue of T HE
JOURNAL (1999;281:862), Congressman Vic Snyder was listed as representing
Arizona when, in fact, he represents Arkansas.
©1999 American Medical Association. All rights reserved.